ArticleNature immunology2025
Spatiotemporal interaction of immune and renal cells controls glomerular crescent formation in autoimmune kidney disease.
Article in Nature immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Autoreactive B cells in systemic lupus erythematosus: insights from integrative multi-omics analyses.Inflammation and regeneration · 2026Review
- A population-scale atlas of blood and tissue in lupus nephritis.bioRxiv : the preprint server for biology · 2026Article
- The continued odyssey to unravel the secrets of kidney inflammation.Nature reviews. Nephrology · 2026Article
- SCALE: unsupervised multiscale domain identification in spatial omics data.Nucleic acids research · 2026Article
- Article
- A stronger type I interferon signature distinguishes ANCA-associated vasculitis phenotypes and predicts kidney prognosis.Kidney international · 2026Article
- Spatial transcriptomics reveals injury-responsive compartments and coordinated immune-fibrotic signaling in ANCA-associated renal vasculitis.Frontiers in immunology · 2026Article
- Single-Cell and Spatial Transcriptomics in Renal Injury and Fibrosis Research.Kidney diseases (Basel, Switzerland)Review
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26 authors.
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Abstract
Rapidly progressive glomerulonephritis (RPGN) is the most aggressive group of autoimmune kidney diseases and is characterized by glomerular crescent formation with proliferation of parietal epithelial cells (PECs). However, the underlying mechanisms of glomerular crescent formation are incompletely understood. Here we provide a high-resolution spatial kidney cell atlas of 57 samples from patients with RPGN (ANCA-associated GN, lupus nephritis and anti-glomerular basement membrane-GN) to characterize the cell signaling pathways in glomerular crescent development. Early platelet-derived growth factor (PDGF) signaling from epithelial and mesangial cells caused PEC activation and proliferation in glomerular crescents, whereas later transforming growth factor (TGF)-β signaling from macrophages, T cells and epithelial and mesangial cells triggered expression of extracellular matrix components in PECs associated with glomerulosclerosis and disease progression. These findings were similar across the different GNs and were functionally validated in experimental GN by PDGF and TGFβ blockade. These results highlight a spatiotemporally conserved progression program into glomerular crescents and sclerosis and indicate new treatment options for autoimmune kidney disease.
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